Maternal inflammation ensuing from high-fat diet (HFD) intake during pregnancy is related to spontaneous preterm birth and respiratory impairment among premature infants. Recently, a circadian aligned dietary intervention referred to as Time-restricted feeding (TRF) has been reported to have beneficial metabolic effects. This study aimed to assess the effects of maternal TRF on fetal lung injury caused by maternal HFD intake. Female Wistar rats were kept on following three dietary regimens; Ad libitum normal chow diet (NCD-AL), Ad libitum HFD (HFD-AL) and Time-restricted fed HFD (HFD-TRF) from 5 months before mating and continued through pregnancy. Fetal lung samples were collected on the embryonic day 18.5, and apoptotic and inflammatory markers were assessed using TUNEL assay, western blotting, and qRT-PCR. Our results showed that TRF considerably prevented maternal HFD-induced apoptosis in fetal lung tissue that corroborated with a reduction in caspase activation and increased levels of anti-apoptotic BCL2 family proteins together with a lower level of ER-stress and autophagy markers including ATF6, CHOP and LC3-II. Besides, fetal lungs from HFD-TRF dams exhibited reduced expression of inflammatory genes that correlated with reduction and apoptotic injury throughout fetal development. Our results thus put forth TRF as a unique non-pharmacological approach to boost perinatal health beneath metabolic stress.
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http://dx.doi.org/10.1016/j.yexmp.2020.104413 | DOI Listing |
Front Microbiol
January 2025
Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Background: Perinatal nicotine exposure (PNE) induces pulmonary dysplasia in offspring and it increases the risk of respiratory diseases both in offspring and across generations. The maternal gut microbiota and its metabolites, such as short-chain fatty acids (SCFAs), can regulate fetal lung development and are susceptible to nicotine exposure. Therefore, modulation of PNE-induced changes in maternal gut microbiota and SCFAs may prevent the occurrence of pulmonary dysplasia in offspring.
View Article and Find Full Text PDFImmunohorizons
January 2025
Section of Infectious Diseases and Epidemiology, Department of Pediatrics, University of Colorado, Aurora, CO, United States.
Respiratory syncytial virus (RSV) is a major contributor to morbidity and mortality in infants. We developed an in vitro model of human respiratory infection to study cellular immune responses to RSV in infants, children, and adults. The model includes human lung epithelial A549 cells or human fetal lung fibroblasts infected with a clinical strain of RSV at a multiplicity of infection of 0.
View Article and Find Full Text PDFJ Matern Fetal Neonatal Med
December 2025
Neonatal Intensive Care Unit, G d'Annunzio University of Chieti, Italy.
Background: Adrenomedullin (AM) is a potent angiogenic, antioxidant and anti-inflammatory peptide protecting the developing lung from injury due to bronchopulmonary dysplasia (BPD) of the preterm infant. At this stage, no data on the potential effects of chorioamnionitis (CA) occurrence and glucocorticoids (GC) administration on AM in developing lungs are still lacking.
Objective: to investigate, in a sheep-based model, the positive/side-effects of combined exposure to CA and GC on AM concentrations measured in bronchoalveolar lavage fluid (BALF).
Fetal Pediatr Pathol
January 2025
Department of Respiratory and Critical Care Medicine, Shenzhen Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, Guangdong, China.
: To explore the clinical value of miR-193a-5p in neonatal acute respiratory distress syndrome (ARDS) and its role in ARDS cell model . : RT-qPCR was utilized to detect miR-193a-5p level. Correlation analysis was implemented to assess the correlation between miR-193a-5p and clinical indicators (IL-6, IL-1β, TNF-α, LUS).
View Article and Find Full Text PDFCureus
December 2024
Laboratory of Histology-Embryology, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, GRC.
Introduction: Maternal infections such as chorioamnionitis could impact fetal lung development by altering cell proliferation and apoptosis. Chorioamnionitis favors the multiple pleiotropic cytokines production such as LIF (leukemia inhibitory factor) and an inflammation-related protein p53. The cytokine production can lead to lung tissue damage and lung disease development.
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